Interestingly, overexpression of the Cav3.1 channel in a Cacna1g transgenic mouse line results in a pure absence epilepsy phenotype with no ataxia or other neurological disturbances [57], suggesting that an increase in Cav3.1 current is sufficient to the pathogenesis of spike-wave seizures. This evidence concerns the gene CACNA1G and cerebellar ataxia.